PubMed · 4021896
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K Stockman, G McKinnon, S Bower, A Davidson. 1985-08-05. Actinobacillus endocarditis.. https://doi.org/10.5694/j.1326-5377.1985.tb122858.x
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Histopathological changes were compared in pigs challenged with Actinobacillus pleuropneumoniae serotype 1 and serotype 5 after inoculation with subunit vaccines. The vaccines consisted of outer membrane protein and/or hemolysin protein isolated from Actinobacillus pleuropneumoniae serotype 1 or both subunits combined. Twenty-seven cross-bred pigs were separated into six groups: Groups I and IV were vaccinated and boostered with 1500 micrograms outer membrane protein; Groups II and V were vaccinated and boostered with 250 micrograms hemolysin protein; Groups III and VI were vaccinated and boostered with a combination of 1500 micrograms outer membrane protein and 250 micrograms hemolysin protein. Groups I, II and III were challenged with A. pleuropneumoniae serotype 1; and Groups IV, V and VI were challenged with A. pleuropneumoniae serotype 5. Groups III and VI demonstrated the least severe lung tissue damage, with significantly lower (P < 0.05) lung involvement as compared to the other groups. Lesions were noted in all six groups. These results showed that complete protection against A. pleuropneumoniae infection was not feasible using a subunit vaccine consisting of just outer membrane protein and hemolysin protein, and that some cross-protection did occur.
Young pigs were immunized with the lung-pathogenic bacterium Actinobacillus (Haemophilus) pleuropneumoniae by aerosol or orally using viable and inactivated bacteria. The cellular changes in the bronchoalveolar lavage (BAL) were studied in repeated lavages after the pigs were infected with live bacteria. The nucleated cells in the BAL were differentiated and lymphocyte subsets determined. There were no major differences between the two routes of immunization or between viable and inactivated bacteria. The immunization induced an increase in all lymphocyte subsets studied and in the appearance of plasma cells and lymphoid blasts. The infection did not cause a further increase except in granulocytes. The lack of a booster-type increase in lymphocytes in the BAL might indicate a different immunologic reaction of the lung or that lymphocytes of the BAL do not represent lung lymphocytes in general. The protective effect of the immunization might be deduced from the increase in lymphocytes after immunization but not from the reaction pattern after infection.
Cross-protection experiments were conducted to determine whether antigenic differences located within the lipopolysaccharides (LPS) of Actinobacillus pleuropneumoniae subtypes 1A and 1B were important with respect to the efficacy of whole cell, formalin-inactivated bacterins. Based on clinical signs, lung lesions scores and mortality rates, pigs immunized with A. pleuropneumoniae subtype 1A were partially protected against severe challenge with both subtypes 1A and 1B. In contrast, 1B vaccinated pigs were not protected against severe challenge with subtype 1A but were partially protected against 1B challenge. Cross-reactive serum antibody levels were measured with an ELISA using outer membranes of subtype 1A or 1B as the coating antigen. Serum antibodies were detected against both subtypes within 2 weeks after the first immunization. Antibody levels increased with time and were generally higher against the homologous subtype coating antigen. We conclude that antigenic variation within a capsular serotype, due to antigenic variation within LPS, can result in the failure of whole cell bacterins to provide protection against challenge with the same capsular serotype. This lack of cross-protection within a capsular serotype provides partial explanation for vaccination failures observed under field conditions.